Mechanism of Action of Cholecystokinin on Colonic Motility in Isolated, Vascularly Perfused Rat Colon.
- Author:
Byeong Seong KO
1
;
Joung Ho HAN
;
Jee In JEONG
;
Hee Bok CHAE
;
Seon Mee PARK
;
Sei Jin YOUN
;
Kae Yol LEE
Author Information
1. Department of Internal Medicine, Cheongju St. Mary's Hospital, Cheongju, Chungcheongbuk-do, Korea.
- Publication Type:Original Article
- Keywords:
Cholecystokinin;
Colon;
Peptide YY
- MeSH:
Animals;
Atropine;
Catheters;
Cholecystokinin;
Colon;
Peptide YY;
Phenobarbital;
Proglumide;
Rats;
Sincalide;
Transducers, Pressure
- From:Journal of Neurogastroenterology and Motility
2011;17(1):73-81
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND/AIMS: It is generally believed that cholecystokinin (CCK) stimulates colonic motility, although there are controversial reports. It has also been suggested that postprandial peptide YY (PYY) release is CCK-dependent. Using a totally isolated, vascularly perfused rat colon, we investigated: (1) the roles of CCK and PYY on colonic motility, (2) to determine if CCK modulates PYY release from the colon to influence the motility and (3) to clarify whether the action of CCK and PYY on colonic motility is mediated via the influence of cholinergic input. METHODS: An isolated whole rat colon was used. Luminal pressure was monitored via microtip catheter pressure transducers from proximal and distal colon. After a control period, CCK-8 or PYY was administerd intraarterially with or without an anti-PYY serum, loxiglumide or atropine at 12, 60 and 240 pM. Each dose was given for a period of 15-minute and the contractile response was expressed as % changes over basal. PYY concentration in the portal effluent was determined by radioimmunoassay. RESULTS: Exogenous CCK-8 increased colonic motility which paralleled the increase in PYY release in the portal effluent. Exogenous PYY also significantly increased colonic motility although it was less potent than CCK. The stimulating effect of CCK-8 was significantly inhibited by an anti-PYY serum, and was completely abolished by loxiglumide, and almost completely abolished by atropine. CONCLUSIONS: CCK increases colonic motility via CCK1 receptor and it is mediated partly by PYY. Cholinergic input is required for the increased motility by either PYY or CCK.
